PTSD and traumatic stress From gene to community and bench to bedside

被引:31
|
作者
Ursano, Robert J. [1 ]
Zhang, Lei [1 ]
Li, He [1 ]
Johnson, Luke [1 ]
Carlton, Janis [1 ]
Fullerton, Carol S. [1 ]
Benedek, Dauid M. [1 ]
机构
[1] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Ctr Study Traumat Stress, Bethesda, MD 20814 USA
关键词
Stress; Posttraumatic stress disorder; PTSD; p11; Glucocorticoid; Cannabinoid; Serotonin receptor; Model; Disaster; Trauma; Traumatic stress; 5-HT2A RECEPTOR-BINDING; SMALLER HIPPOCAMPAL VOLUME; MENTAL-HEALTH PROBLEMS; LEARNED HELPLESSNESS; GLUCOCORTICOID-RECEPTORS; SEROTONERGIC MODULATION; ACUTE AFTERMATH; CORTISOL-LEVELS; NEURAL SYSTEMS; DISORDER;
D O I
10.1016/j.brainres.2009.03.030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Individuals and communities are exposed to traumatic events, those that are accidents or naturally occurring and those that are intentional or human made. Although resilience is the expected response, for some, posttraumatic stress disorder may be the outcome. Brain models of PTSD require understanding the phenomenology of the disorder and the brain "break down" that occurs. Among several models, importantly, is the perspective that PTSD is a "forgetting" disorder. Other elements in the onset and triggers of PTSD can identify further models to examine at the bench. New studies of the 5-HT2A receptor, the glucocorticoid receptor, p11, mitochondrial genes and cannabinoids are bringing new perspectives to understanding brain function in PTSD. Effective treatments indicate areas for bench research on the mechanisms of the disorder. Published by Elsevier B.V.
引用
收藏
页码:2 / 12
页数:11
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